Summary Since platelet aggregation is dependent on the presence of functional GP IIb/IIIa receptors and since this receptor is unique to platelets, functional interaction with this receptor by antagonistic drugs allows pharmacologic abrogation of platelet aggregation. The first GP IIb/IIIa receptor blocking agent was the chimeric Fab antibody c7E3 also known as abciximab. Further low molecular GP IIb/IIIa receptor blocking agents have been designed which are based on the tripeptidic arginine-glycine-aspartic acid (RGD) or lysine-glycine-aspartic acid (KGD) binding sequences (Eptifibatide) or which chemically mimic these tripeptides (e.g. Tirofiban, Lamifiban, Lefradafiban, Orbofiban and Xemilofiban). In large-scale clinical trials, clear-cut benefits in patients having received GP IIb/IIIa receptor blocking agents have been shown for: (1) unstable angina with immediate or early angioplasty or primary stabilization; (2) primary angioplasty in acute myocardial infarction; and (3) routine low- and high-risk coronary angioplasty in patients, independent of whether they are treated with plain balloon dilatation, rotablation, directional artherectomy, and/or coronary stenting. The benefits encountered when GP IIb/IIIa platelet receptor blockers are given as a conjunct to thrombolytic agents are less clear-cut and may be offset by an increased bleeding hazard. Even though the GP IIb/IIIa receptor blocker abciximab may have a slight benefit as a disintegrating agent, its use in patients with acute myocardial infarction cannot substitute for potent thrombolytic agents. The down side of this new class of powerful antithrombotic agents is an increased risk of bleeding, mainly at puncture sites, without an increased risk for hemorrhagic strokes. This risk is acceptable, as long as concomitant heparin is appropriately given in low doses. A 1–2% risk of severe thrombocytopenia ( 3 ) may require immediate cessation of drug infusion and the substitution of platelet concentrates. A fraction of thrombocytopenias, however, may be pseudo-thrombocytopenias with platelet clumping due to EDTA used for anticoagulation in blood collecting tubes. If a severe thrombocytopenia is encountered, repeat platelet counting from citrated or heparinized blood and a review of the peripheral blood film are advised before specific treatment measures are taken.